Animal Models of Cardiac Disease and Stem Cell Therapy

Ou, Lailiang; Li, Wenzhong; Liu, Yi; Zhang, Yue; Shen, Jie; Kong, Deling; Steinhoff, Gustav; Ma, Nan

doi:10.2174/1874192401004010231

Cited by 35 publications

(19 citation statements)

References 149 publications

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“…Use of isoproterenol (ISO), a β adrenergic agonist and a synthesized catecholamine, has been done since long time for studying the efficacy of newer molecules against MI in animal model [13]. ISO has been known to produce MI in quantity above therapeutic dose, through production of elevated levels of free radicals by undergoing oxidation, and thereby induce cytotoxicity [14,15]. These oxidative remainders are known for further modulation of the myocardial tissue functionality.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective Effect of Rhapontigenin in Isoproterenol-Induced Myocardial Infarction in a Rat Model

Fan

2019

Pharmacology

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Background/Aims: Rhapontigenin (RPG) is a stilben derivative and is known to bear several effects such as antiallergic, anticoagulative, hypoglycemic, antiangiogenic, and purgative. The investigation was conducted to evaluate the cardioprotective efficacy of RPG in rats having acute myocardial infarction (MI) induced by isoproterenol (ISO). Methods: Animals were divided into 6 groups: group I (control group), group II (ISO-treated), group III (1.0 mg/kg/day RPG and ISO-treated), group IV (2.5 mg/kg/day RPG and ISO-treated), group V (5.0 mg/kg/day RPG and ISO-treated), and group VI (treated with RPG 5.0 mg/kg/day). Various cardiac stress markers, including infarct size and heart/body weight index, were investigated in animals with ISO-induced MI, such as inducible nitric oxide synthase (iNOS), creatinine kinase (CK), lactate dehydrogenase (LD), cardiac troponin-T (CTT), superoxide dismutase (SOD), and malondialdehyde. INOS, p38, caspase-3, and connexin 43 expressions were analyzed in animals. Inflammatory mediators, tissue necrosis factor-α (TNF-α) and interleukin-6 (IL-6), were detected in serum of experimental animals. Results: Group I animals indicated normal levels of biochemical parameters, whereas group II animals indicated high levels of these parameters and successful induction of MI. Pretreatment of animal groups III, IV, and V with RPG revealed amelioration of infarct size, heart/body weight index, CK, LD, CTT in rats, whereas group VI animals were treated only with RPG (5.0 mg/kg/day) and not with ISO. Levels of TNF-α, IL-6, MD, SOD, p38, and iNOS expressions were significantly downregulated by RPG administration (5.0 mg/kg/day). Conclusion: RPG ameliorates MI caused by ISO in rats and provides cardioprotective effect, via anti-inflammatory, antioxidant, and antiapoptotic effect.

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Section: Introductionmentioning

confidence: 99%

Cardioprotective Effect of Rhapontigenin in Isoproterenol-Induced Myocardial Infarction in a Rat Model

Fan

2019

Pharmacology

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“…Previous studies have indicated that cTnI is a protein associated with the myocyte contractile apparatus, which will be released into the serum when myocytes are injured and can serve as a marker of myocyte injury [21]. cTnI is highly sensitive and specific for myocarditis in mice 17-21 days after MyHCa immunization [22]. We found that insulin treatment lowered serum cTnI levels of EAM mice significantly on days 14 (P < 0·05) and 21 (P < 0·05) compared with the saline-treated group.…”

Section: Discussionmentioning

confidence: 99%

Insulin promotes T cell recovery in a murine model of autoimmune myocarditis

Zhang

Zhuang

Geng

et al. 2012

Clinical and Experimental Immunology

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SummaryGlucose-insulin-potassium (GIK) is a useful adjunct to myocarditis. Besides its essential action in energy metabolism, insulin also exerts an antiinflammatory effect. This study investigated the effect of insulin on myocardial inflammation in experimental autoimmune myocarditis (EAM) in mice and its potential role in T cell regulation. Mice were divided randomly into a normal control group, a saline-treated EAM group and an insulin-treated EAM group. The histopathological changes of myocardium, a-myosin heavy chain (MyHCa)614-629 antigen-specific autoantibody titre, the serum level of cardiac troponin I (cTnI), mitogen-activated protein kinase (MAPK) family members' activity and content were measured. Furthermore, the phenotype of T lymphocyte subsets in splenocytes was analysed to evaluate the immune status of mice. Insulin reduced serum cTnI of EAM mice on days 14 and 21 (P < 0·05) after immunization, with no changes in blood glucose and autoantibody production. Western blot revealed that extracellular signalregulated protein kinase (ERK1/2) may be a determining factor in this process. Total ERK1/2 and phospho-ERK1/2 (p-ERK1/2) were both up-regulated in insulin-treated mice after immunization. We also found that insulin treatment promoted T cell recovery without changing the naive-tomemory T-cell ratio; in particular, CD3+ T cells in insulin-treated mice proliferated more vigorously than in control mice (P < 0·05). We report here for the first time that insulin alleviates myocarditis in the EAM model. These data show that insulin has a direct effect on T cell proliferation in EAM. It is possible that GIK or insulin may assist T cell recovery towards normal in myocarditis, especially for diabetic or hyperglycaemic patients.

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“…In MI-Magnet + MNBs/Ad hVEGF , MI-MNBs, and MI-Magnet + MNBs/Ad GFP groups, MI was induced as described earlier [24]–[26]. Briefly the left anterior descending coronary artery(LAD)was ligated permanently.…”

Section: Methodsmentioning

confidence: 99%

Targeted Delivery of Human VEGF Gene via Complexes of Magnetic Nanoparticle-Adenoviral Vectors Enhanced Cardiac Regeneration

Zhang

et al. 2012

PLoS ONE

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This study assessed the concept of whether delivery of magnetic nanobeads (MNBs)/adenoviral vectors (Ad)–encoded hVEGF gene (AdhVEGF) could regenerate ischaemically damaged hearts in a rat acute myocardial infarction model under the control of an external magnetic field. Adenoviral vectors were conjugated to MNBs with the Sulfo-NHS-LC-Biotin linker. In vitro transduction efficacy of MNBs/Ad–encoded luciferase gene (Adluc) was compared with Adluc alone in human umbilical vein endothelial cells (HUVECs) under magnetic field stimulation. In vivo, in a rat acute myocardial infarction (AMI) model, MNBs/AdhVEGF complexes were injected intravenously and an epicardial magnet was employed to attract the circulating MNBs/AdhVEGF complexes. In vitro, compared with Adluc alone, MNBs/Adluc complexes had a 50-fold higher transduction efficiency under the magnetic field. In vivo, epicardial magnet effectively attracted MNBs/AdhVEGF complexes and resulted in strong therapeutic gene expression in the ischemic zone of the infarcted heart. When compared to other MI-treated groups, the MI-M+/AdhVEGF group significantly improved left ventricular function (p<0.05) assessed by pressure-volume loops after 4 weeks. Also the MI-M+/AdhVEGF group exhibited higher capillary and arteriole density and lower collagen deposition than other MI-treated groups (p<0.05). Magnetic targeting enhances transduction efficiency and improves heart function. This novel method to improve gene therapy outcomes in AMI treatment offers the potential into clinical applications.

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Animal Models of Cardiac Disease and Stem Cell Therapy

Cited by 35 publications

References 149 publications

Cardioprotective Effect of Rhapontigenin in Isoproterenol-Induced Myocardial Infarction in a Rat Model

Cardioprotective Effect of Rhapontigenin in Isoproterenol-Induced Myocardial Infarction in a Rat Model

Insulin promotes T cell recovery in a murine model of autoimmune myocarditis

Targeted Delivery of Human VEGF Gene via Complexes of Magnetic Nanoparticle-Adenoviral Vectors Enhanced Cardiac Regeneration

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